Hypertensive diseases in pregnancy

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Chapter 14 Hypertensive diseases in pregnancy

CHAPTER CONTENTS

Classification 117

Gestational hypertension 117
Pre-eclampsia 117
Chronic hypertension 118
Pre-eclampsia superimposed on chronic hypertension 118
Gestational hypertension 118
Pre-eclampsia 119

Pathogenesis 119
Prevention 119
Management 119
Eclampsia 120

Pathophysiology 120
Clinical picture 120
Management of eclampsia 120
Medical and drug treatment 121
Prognosis in pre-eclampsia and eclampsia 121
Chronic hypertension 121

Pathophysiology 121
Treatment 122
Renal disease in pregnancy 122

Between 5 and 8% of pregnancies are complicated by hypertensive diseases. These are gestational hypertension, pre-eclampsia, chronic hypertension, essential and secondary and superimposed pre-eclampsia.

CLASSIFICATION

Gestational hypertension

Gestational hypertension is classified as hypertension that arises after 20 weeks’ gestation without any of the other features of pre-eclampsia and resolves within 3 months of delivery.

Pre-eclampsia

Pre-eclampsia is a multisystem disorder; hypertension is usually the first manifestation, followed by proteinuria. The clinical diagnosis of pre-eclampsia requires the onset after 20 weeks’ gestation of hypertension and one or more of:

• Proteinuria – >300 mg/24 h or urine protein/creatinine ratio >30 mg/mmol
• Renal insufficiency – serum/plasma creatinine >0.09 mmol/L or oliguria
• Liver disease – raised serum transaminases and/or severe epigastric/right upper quadrant pain
• Neurological problems – convulsions (eclampsia); hyperreflexia with clonus; severe headaches with hyperreflexia; persistent visual disturbances (scotomata)
• Haematological disturbances – thrombocytopenia; disseminated intravascular coagulation; haemolysis
• Fetal growth restriction.

The hypertension of pre-eclampsia returns to normal within 3 months of delivery.

Chronic hypertension

• Essential hypertension: blood pressure ≥140 mmHg systolic and/or ≥90 mmHg diastolic (K5) prior to conception or in the first half of pregnancy without an apparent underlying cause.
• Secondary hypertension: hypertension associated with renal, renovascular and endocrine disorders and aortic coarctation.

Pre-eclampsia superimposed on chronic hypertension

This is diagnosed when one or more of the systemic features of pre-eclampsia develops after 20 weeks, i.e. in addition to a rise in blood pressure and/or a sudden increase in protein excretion.

GESTATIONAL HYPERTENSION

Pregnancies complicated by gestational hypertension have a good prognosis. The blood pressure should be carefully monitored and this can normally be done in a Day Assessment Unit or with ambulatory home blood pressure monitoring. Careful surveillance should be maintained to exclude the development of pre-eclampsia.

If the blood pressure exceeds 140/90 then antihypertensive therapy, as detailed in Table 14.1, is commenced, with the objective of maintaining the systolic pressure between 110 and 140 mmHg and the diastolic between 80 and 90 mmHg.

Table 14.1 Summary of the management of pregnancy-induced hypertension

Classification Observations Treatment
Gestational hypertension Report rise in blood pressure or excessive weight gain to obstetrician Assess in day assessment unit or ambulatory blood pressure monitoring at home
Moderate pre-eclampsia
In hospital:
Four-hourly recording of the blood pressure
Twice-daily urine testing for protein
Regular observation of the patient’s condition, including fluid intake and output
Bed rest, but toilet privileges allowed

Admit to hospital
Sedation (if indicated)
Methyldopa (starting) 250 mg two to three time daily increasing to max. 3 g daily
Labetalol (starting) 100 mg twice daily or atenolol (starting) 100 mg in evening or oxprenolol (starting) 20 mg three times daily or methyldopa (starting) 250 mg three times daily
Nifedipine 10–20 mg twice daily to max. 40 mg b.d.
Severe pre-eclampsia
Two-hourly blood pressure recording for 6 hours, then 4-hourly
Urine testing for protein twice daily
Fluid intake and output recorded
Careful observation of the patient for the signs of imminent eclampsia
Complete bed rest for 24 hours, thereafter possible toilet privileges
Admit to hospital
Depending on the severity of the illness give:

a. Magnesium sulphate (see p. 121).
b. Hydralazine – start 5–10 mg IV slowly, repeat 20–30 min. Continue infusion 50–300 μg/min, rate to keep BP around 140/90

Imminent eclampsia
The patient requires careful systematic observation as eclampsia is a possible outcome
The blood pressure requires frequent estimation, at intervals determined by the obstetrician
Fluid intake and urinary output must be measured meticulously, and the urine tested quantitatively for protein
Magnesium sulphate (see p. 121).
Hydralazine intravenously
Caesarean section

PRE-ECLAMPSIA

Pathogenesis

The aetiology of pre-eclampsia is not known, but there is evidence that the disorder has a genetic basis as the daughters and sisters of women who had pre-eclampsia are at increased risk. Late in the first trimester the secondary invasion of maternal spiral arteries by trophoblasts is impaired, so that they remain high-resistance vessels, which consequently leads to impairment of placental function. As pregnancy advances, placental hypoxic changes induce proliferation of cytotrophoblasts and thickening of the trophoblastic basement membrane, which may affect the metabolic function of the placenta. Normally the endothelial cells secrete vasodilator substances (including nitric oxide). Damaged cells secrete less vasodilators. In consequence, endothelial cells of the placenta secrete less vasodilator prostacyclin and the platelets more thromboxane, leading to generalized vasoconstriction and decreased aldosterone secretion. The results of these changes are maternal hypertension, a 50% reduction in placental perfusion, and a reduced maternal plasma volume. If the vasospasm persists trophoblastic epithelial cell injury may occur, and trophoblast fragments are then carried to the lungs, where they are destroyed, releasing thromboplastins. In turn, thromboplastins cause intravascular coagulation and deposition of fibrin in the glomeruli of the kidneys (glomerular endotheliosis), which reduces the glomerular filtration rate and indirectly increases vasoconstriction. In advanced, severe cases fibrin deposits occur in vessels of the central nervous system, leading to convulsions.

Prevention

Prophylactic aspirin therapy given to women at high risk of developing pre-eclampsia (essential hypertension, type 1 diabetes, previous severe pre-eclampsia) results in a modest reduction (OR 0.87; 95% CI 0.79–0.96). Calcium supplementation in at-risk women is associated with a 50% reduction in gestational hypertension and pre-eclampsia. Antioxidant therapy (vitamins C and E) has not been shown to be effective for prevention of pre-eclampsia.

Management

The management of pre-eclampsia is shown in Table 14.1. The basic principles of maternal treatment are to control the blood pressure and to prevent convulsions.

For the fetus the aim of treatment is to permit continued growth until it is sufficiently mature to survive outside the uterus, or until the risk of intra-uterine death is estimated to be greater than that of extra-uterine death. The duration of treatment depends on:

• The severity of pre-eclampsia
• The duration of the pregnancy
• The patient’s response to treatment.

There is no cure for pre-eclampsia except to terminate the pregnancy and deliver the fetus and placenta. The treatment is merely to buy time so that the fetus becomes more mature in the uterus.

Pre-eclampsia diagnosed before week 32 of pregnancy

Before the 32nd week of pregnancy the objective is to keep the fetus in utero until the 35th week or longer. Fetal wellbeing is monitored by daily fetal movement counts, or 3 cardiotocograph examinations per week (see p. 153). Two sinister signs are slow fetal growth detected by serial ultrasound examinations, and abnormal Doppler umbilical blood flow measurements.

Platelet counts are made at intervals in cases of severe pre-eclampsia. In most cases a reduced platelet count returns to normal after the birth, but a few patients who have severe pre-eclampsia complain of upper abdominal pain, nausea or vomiting. If the platelet count is less than 100 000 the woman may have the HELLP syndrome (haemolysis, elevated liver enzymes, low platelets). Treatment consists of correcting the thrombocytopenia and delivering the fetus; systemic high-dose corticosteroids can shorten the recovery phase.

If the pre-eclampsia worsens the pregnancy must be terminated, usually by caesarean section.

Pre-eclampsia diagnosed between the 32nd and 35th weeks of pregnancy

Pre-eclampsia diagnosed between the 32nd and 35th weeks is managed in the same way as before the 32nd week, but should delivery of the fetus be indicated the choice is caesarean section or induction of labour.

Pre-eclampsia diagnosed after the 35th week of pregnancy

Pre-eclampsia diagnosed after the 35th week of pregnancy should be controlled rapidly and labour induced or a caesarean section performed, depending on the condition of the fetus and the state of the cervix.

Women with pre-eclampsia should not be allowed to exceed full term, as the risk of intra-uterine death increases after term.

Care after birth

The woman needs to have close monitoring of her blood pressure until it resolves. If the blood pressure remains high antihypertensive agents should be continued. Proteinuria often persists for longer and is of little consequence. One-third of the women will have non-proteinuric hypertension in a subsequent pregnancy, but the rate of recurrence of severe pre-eclampsia is less than 5%.

If severe pre-eclampsia presents before 34 weeks’ gestation a careful search for an underlying medical disorder, such as renal disease, should be made.

ECLAMPSIA

The purpose of treating hypertensive disorders in pregnancy is to prevent eclampsia. The word arises from the Greek for ‘like a flash of lightning’, and this is how the disease may occur.

Eclampsia is characterized by convulsions and coma, which usually occur in patients who have severe pre-eclampsia or imminent eclampsia, and in patients in whom gestational proteinuria has been superimposed on chronic hypertension. In 10–30% of women there are no warning signs, the fits occurring ‘like a flash of lightning’. With better antenatal care and early recognition and treatment of pre-eclampsia and chronic hypertension, the incidence of eclampsia has fallen. In developed countries eclampsia occurs in 1 : 2000 pregnant women, but in the developing countries the incidence is higher.

Pathophysiology

The changes that occur in severe pre-eclampsia are more marked in eclampsia: vasospasm is intense, with tissue hypoxia; the glomerular filtration rate is further reduced and urinary output falls; intracellular water retention impedes cellular metabolism and cerebral oedema may occur; blood viscosity increases, platelet levels fall and coagulation defects arise.

Clinical picture

The convulsion is preceded by a disorientation stage during which the woman becomes restless, twitches, and develops spasmodic respiration. Within a minute she passes into the tonic stage of the convulsion: her back arches, her hands clench, she grimaces, her breathing ceases and she becomes cyanosed. In this stage she may bite her tongue. She then passes into the clonic stage of the convulsion, when her body jerks uncontrollably, frothy saliva may fill her mouth and her breathing becomes stertorous. Finally, she becomes comatose (Fig. 14.1). The coma may persist for an hour or longer, or recurrent convulsions may occur.

image

Fig. 14.1 Eclampsia. The face of an eclamptic patient.

The convulsions occur in late pregnancy in 40% of cases, intrapartum in 30%, and a few hours after the birth in 30%.

Management of eclampsia

The aims of treatment are:

• To control the fits by relieving the generalized vascular spasm and decreasing the sensitivity of the brain to stimuli
• To reduce the blood pressure to prevent cerebral haemorrhage
• To deliver the fetus.

Midwifery care

The quality of the midwifery care of an eclamptic patient is crucial. The patient is nursed on her side, with her head and shoulders raised, and a catheter is inserted into her bladder. The attending midwives must:

• Detect any changes presaging a second convulsion
• Prevent the woman injuring herself during a convulsion
• Provide continuous oxygen
• Keep the mouth and fauces clear of any saliva by suction
• Monitor vital signs and urinary output.

Medical and drug treatment

Drug treatment – magnesium sulphate

Magnesium reduces the risk of recurrent seizures by relieving vasospasm and inducing cerebral vascular dilatation. It increases the release of prostacyclin, improving uterine blood flow, inhibits platelet activation and protects endothelial cells from injury.

Magnesium sulphate may be given intravenously or by deep intramuscular injection (Box 14.1). The intravenous route is preferred, as intramuscular injections are painful and are followed, in 5% of cases, by deep abscess formation.

Box 14.1 Magnesium sulphate treatment for eclampsia

Loading dose

MgSO4 4 g intravenously over 5 to 15 minutes

Maintenance dose

MgSO4 1 g per hour in solution of 5 g in 500 mL normal saline

The regimen is as follows:

• Loading dose when the eclamptic patient is first seen: MgSO4 4 g IV over 10–15 minutes, followed by MgSO4 1 g/h (as an infusion of MgSO4 5 g in 500 mL of normal saline).
• Continuing treatment: rate of infusion to provide 1 g/h until 24 hours have passed since the last seizure, or the woman has given birth.
• Magnesium is excreted by the kidneys and is a smooth muscle relaxant. It is important that tendon reflexes, respiratory rate (>16/min) and urine output (>25 mL/h) are monitored to detect magnesium toxicity. If this occurs the management is:

• Respiratory arrest: intubate, ventilate, and stop the MgSO4 infusion. Give 1 g calcium gluconate IV (the antidote to magnesium toxicity)
• Respiratory depression: give oxygen by mask, calcium gluconate 1 g IV, and maintain a clear airway
• Absent patellar reflexes: if respiration is normal, stop the MgSO4 infusion until reflexes return. If respiration is depressed, treat for this condition
• Poor urinary output (<100 mL in 4 hours): if there are no other signs of magnesium toxicity, reduce the rate of the IV infusion to 0.5 g/h and monitor fluid balance.

Antibiotics should be prescribed.

If cardiac failure occurs, furosemide (frusemide) 20 mg may be given intravenously, but because of the hypovolaemia it should be used with care.

Medical treatment

Once good control of the blood pressure and the convulsions has been obtained the pregnancy should be terminated. Depending on the period of the gestation, the health (alive or dead) of the fetus and its presentation, and on the condition of the cervix, delivery may be effected by caesarean section or labour may be induced using prostaglandins or by amniotomy. In most cases of eclampsia the induction of labour is followed rapidly by the birth of the infant. As postpartum haemorrhage may occur, prophylactic intravenous Syntocinon should be given on the birth of the infant. The patient should continue to be monitored at least for the first 4 days of the puerperium.

Prognosis in pre-eclampsia and eclampsia

In developing countries it is estimated that 50 000 maternal deaths annually are due to pre-eclampsia. Today few women in the developed countries should die from severe pre-eclampsia or from eclampsia. Most deaths are from cerebral haemorrhage or cardiac failure.

CHRONIC HYPERTENSION

Most women with chronic hypertension have been diagnosed before pregnancy; a few are found to be hypertensive at the first antenatal visit. In the absence of a secondary cause for hypertension (for example renal artery stenosis or phaeochromocytoma), a raised blood pressure (>140/90 mmHg) which persists and is present before pregnancy or detected before the 20th gestational week, is diagnostic of essential hypertension. It is important to remember that the small physiological fall in blood pressure in the first half of pregnancy may be exaggerated in women who have chronic hypertension, and some cases may be missed.

Essential hypertension complicates 1–3% of pregnancies and is more frequent in women over the age of 35.

Pathophysiology

The generalized vasospasm of essential hypertension is counterbalanced by an increased stroke volume and heart rate, which maintains an adequate blood flow to most organs with the exception of the uterus. Although uterine blood flow is increased in normal pregnancy the increase is less in women who have essential hypertension, and the higher the blood pressure the less the increase. This may reduce fetal growth and increase perinatal loss.

Pregnancy affects the course of essential hypertension. In 60% of affected women a rise in blood pressure occurs, and in 30% significant proteinuria (>300 mg/L) is detected. The changes usually occur after the 30th week of pregnancy. Essential hypertension with superimposed proteinuria is indistinguishable from severe pre-eclampsia.

Treatment

The aims of treatment are:

• To obtain and to maintain as good a blood supply to the uterus as possible
• To control the level of the blood pressure and prevent the superimposition of proteinuria
• To terminate the pregnancy if the patient’s condition deteriorates markedly, or if the fetus fails to grow adequately in the last quarter of pregnancy.

Maintenance of uterine blood supply

Usually the woman is instructed to rest more to improve the uterine blood supply.

Control of the hypertension

Most patients will be taking an antihypertensive drug and a physician should be consulted to confirm that the drug is required and that it is safe to be given during pregnancy. Diuretics should be avoided as these agents reduce plasma volume and uteroplacental blood flow. Most experience has been obtained using methyldopa, but it appears that β-blockers such as atenolol and labetalol, and calcium-channel blockers (e.g. nifedipine) are safe. Angiotensin-converting enzyme (ACE) inhibitors should be avoided because of their potential teratogenicity.

Avoidance of problems

The woman should be seen more frequently during the antenatal period, the frequency depending on the severity of the hypertension. Her lifestyle should be checked, and if she is obese a reduction diet should be prescribed. If the fetus shows signs of growth restriction, biophysical tests for fetal wellbeing should be started (Ch. 20), and if conditions deteriorate induction of labour should be discussed with the patient. It is safer for the fetus to be born earlier rather than later, and the patient should not become postdate as the risk of perinatal loss increases.

RENAL DISEASE IN PREGNANCY

Less than 0.2% of pregnant women, and less than 5% of women with hypertension in pregnancy, have renal disease. In most cases the diagnosis is known beforehand, but routine examination of a midstream specimen of urine (which is made to detect asymptomatic bacteriuria) may occasionally detect an affected woman. Most affected women have no impairment of renal function, which is tracked by periodic serum creatinine measurements. If the level rises to more than 0.18 mmol/L and there is evidence of poor fetal growth, either renal dialysis or induction of labour should be performed after consultation with a renal physician.

Women with a renal transplant have a 90% likelihood of a successful pregnancy outcome providing that the woman’s renal function has been stable for 2 years before conception, that she is normotensive or her hypertension is well controlled and she has minimal proteinuria. Close monitoring of both renal and fetoplacental function is required and delivery by caesarean section needs only to be performed for obstetric indications.

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